The prevailing model of amnesia holds that it depends on damage to a group of loosely related structures, collectively called the medial temporal lobe (MTL). One influential theory holds that these areas work together as a single functional unit. According to this theory, the structures in the MTL store the memory of specific objects, facts and events. We have developed a competing hypothesis, which holds that different structures within the MTL have specialized functions, and that their collective functions extend beyond those assigned to the MTL by the prevailing model. In the last year we investigated the neural underpinnings of stimulus recognition memory. Specifically, we investigated the contribution of the amygdala, a structure in the medial temporal lobe, to this ability. Dual-process accounts of stimulus recognition posit two memory processes: slow but detailed recollection, and quick but vague familiarity. It has been proposed, based on prior rodent work, that the amygdala is critical for the familiarity aspect of item recognition. Here, we evaluated this proposal in animals with selective bilateral excitotoxic amygdala damage. We used a variety of visual memory tests designed to assess different aspects of familiarity, all administered on touchscreen computers. Specifically, we assessed animals tendencies to make low-latency false alarms, to make false alarms to recently-seen lures, to produce curvilinear ROC curves, and to discriminate stimuli based on repetition across days. Across these metrics, monkeys with selective amygdala damage performed like unoperated control monkeys. However, amygdala damage did produce an anticipated deficit in rapid stimulus-reward learning in a three-arm-bandit gambling task, verifying the effectiveness of the lesions. Together, these results contradict prior rodent work and suggest that the amygdala is not critical for the familiarity aspect of item recognition.